Left ventricular hypertrophy (LVH), hypertension and atherosclerotic coronary arterial disease commonly coexist. Logical decisions regarding whether, and to what level, to reduce afterload in hypertensive patients during acute ischemia are difficult. Systemic hypertension increases both left ventricular (LV) wall tension and oxygen consumption but also increases coronary perfusion pressure. Likewise, LVH tends to normalize increased LV wall stress but the cross-sectional area of the coronary bed supplying the hypertrophied mass of myocardium does not increase proportionately. Hence, the hypertrophied myocardium may be more vulnerable to an ischemic insult. In order to further study these problems, I propose to produce left ventricular hypertrophy by a pressure or volume overload in mongrel dogs. Pressure overload will be produced by the surgical creation of renovascular hypertension; volume overload will be produced by the creation of complete heart block. A third group will consist of normotensive controls. After 5-6 weeks LV mass will increase by 50% on average. After LVH has developed dogs will be re-operated on and pulse-transit piezo-electric crystals imbedded in up to 6 regions of the LV wall to measure segmental function. An occluding balloon will be placed around the left anterior descending artery (LAD). After 1-2 weeks of recovery LAD occlusion will be produced in awake, unsedated dogs. Regional myocardial blood flows will be measured with 9 mu radio-labeled microspheres. Regional function, regional flow and hemodynamics will be studied serially for up to 4 weeks in all dogs. After sacrifice of the animal, relative and absolute sizes of LAD and circumflex beds will be measured by infusing the LAD with triphenyl tertrazolium chloride and the circumflex with blue dye. Infarct size, expressed in this manner, can be more efficiently and rationally compared between groups of animals since the variability in infarct size arising from differences in collateral circulation is reduced. Infarct size can then be expressed as percent LAD bed at risk. The extent of histological necrosis at each crystal site will also be determined.